Pulmonary complications associated with veno-arterial extra-corporeal membrane oxygenation: a comprehensive review

Abstract

Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is a life-saving technology that provides transient respiratory and circulatory support for patients with profound cardiogenic shock or refractory cardiac arrest. Among its potential complications, VA-ECMO may adversely affect lung function through various pathophysiological mechanisms. The interaction of blood components with the biomaterials of the extracorporeal membrane elicits a systemic inflammatory response which may increase pulmonary vascular permeability and promote the sequestration of polymorphonuclear neutrophils within the lung parenchyma. Also, VA-ECMO increases the afterload of the left ventricle (LV) through reverse flow within the thoracic aorta, resulting in increased LV filling pressure and pulmonary congestion. Furthermore, VA-ECMO may result in long-standing pulmonary hypoxia, due to partial shunting of the pulmonary circulation and to reduced pulsatile blood flow within the bronchial circulation. Ultimately, these different abnormalities may result in a state of persisting lung inflammation and fibrotic changes with concomitant functional impairment, which may compromise weaning from VA-ECMO and could possibly result in long-term lung dysfunction. This review presents the mechanisms of lung damage and dysfunction under VA-ECMO and discusses potential strategies to prevent and treat such alterations.

Keywords: Cardiogenic shock; Extracorporeal membrane oxygenation; Lung injury.

Fig. 1

Main VA-ECMO-induced mechanisms of lung damage and dysfunction. Left side: SIRS is initiated by the blood contact with the circuitry surface. It activates humoral cascades, platelets, and leukocytes, leading eventually to EC injury and activated PMN sequestration into the lung parenchyma. Right side: EC injury favors fluid infiltration into both alveolar space and lung parenchyma, leading to pulmonary edema, which is aggravated by the increase of pulmonary vein pressure. Alveolar edema and decreased pulmonary artery perfusion lead to lung parenchymal ischemia which in turn maintains chronic inflammation and promotes neoangiogenesis and fibrosis generation

Fig. 2

The watershed. a Axial. b Sagittal. Contrast in the aorta indicates blood flow from the VA-ECMO arterial cannula, whereas absence of contrast within the ascending aorta indicates blood flow from the native heart. The level of blood mixing in the thoracic aorta represents the VA-ECMO watershed (arrows)

Fig. 3

Veno-veno-arterial ECMO. Oxygenated blood is propelled through both the femoral arterial cannula and the additional jugular cannula providing oxygenated blood directly into the right-heart chambers and consequently into the left atrium. This setting permits to wean progressively the arterial cannula in order to switch to veno-venous ECMO